scholarly journals Differential hippocampal gene expression and pathway analysis in an etiology-based mouse model of major depressive disorder

2015 ◽  
Vol 168 (4) ◽  
pp. 316-316 ◽  
Author(s):  
George S. Zubenko ◽  
Hugh B. Hughes ◽  
Rick M. Jordan ◽  
James Lyons-Weiler ◽  
Bruce M. Cohen
Keyword(s):  
Gene Expression ◽  
Major Depressive Disorder ◽  
Mouse Model ◽  
Depressive Disorder ◽  
Pathway Analysis ◽  
Major Depressive

scholarly journals Cortical structural differences in major depressive disorder correlate with cell type-specific transcriptional signatures

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Jiao Li ◽  
Jakob Seidlitz ◽  
John Suckling ◽  
Feiyang Fan ◽  
Gong-Jun Ji ◽  
...  
Keyword(s):  
Gene Expression ◽  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Structural Changes ◽  
Brain Regions ◽  
Cell Type ◽  
Major Depressive ◽  
Structural Differences ◽  
Neuroimaging Data ◽  
Cell Type Specific

AbstractMajor depressive disorder (MDD) has been shown to be associated with structural abnormalities in a variety of spatially diverse brain regions. However, the correlation between brain structural changes in MDD and gene expression is unclear. Here, we examine the link between brain-wide gene expression and morphometric changes in individuals with MDD, using neuroimaging data from two independent cohorts and a publicly available transcriptomic dataset. Morphometric similarity network (MSN) analysis shows replicable cortical structural differences in individuals with MDD compared to control subjects. Using human brain gene expression data, we observe that the expression of MDD-associated genes spatially correlates with MSN differences. Analysis of cell type-specific signature genes suggests that microglia and neuronal specific transcriptional changes account for most of the observed correlation with MDD-specific MSN differences. Collectively, our findings link molecular and structural changes relevant for MDD.

scholarly journals Differential gene expression in patients with subsyndromal symptomatic depression and major depressive disorder

PLoS ONE ◽  
2017 ◽  
Vol 12 (3) ◽  
pp. e0172692 ◽  
Author(s):  
Chengqing Yang ◽  
Guoqin Hu ◽  
Zezhi Li ◽  
Qingzhong Wang ◽  
Xuemei Wang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Differential Gene Expression ◽  
Major Depressive ◽  
Differential Gene

Glucocorticoid Signaling in Stress-Related Psychiatric Disorders Uncovered by Dexamethasone-Induced Gene Expression

2017 ◽  
Author(s):  
Andreas Menke
Keyword(s):  
Gene Expression ◽  
Major Depressive Disorder ◽  
Major Depression ◽  
Depressive Disorder ◽  
Glucocorticoid Receptor ◽  
Psychiatric Disorders ◽  
Hpa Axis ◽  
Stimulation Test ◽  
Major Depressive ◽  
Depressed Patients

Major depressive disorder (MDD) is a common, serious and in some cases life‐threatening condition and affects approximately 350 million people globally (Otte et al., 2016). The magnitude of the clinical burden reflects the limited effectiveness of current available therapies. The current prescribed antidepressants are based on modulating monoaminergic neurotransmission, i.e. they improve central availability of serotonin, norepinephrine and dopamine. However, they are associated with a high rate of partial or non-response, delayed response onset and limited duration. Actually more than 50% of the patients fail to respond to their first antidepressant they receive. Therefore there is a need of new treatment approaches targeting other systems than the monoaminergic pathway. One of the most robust findings in biological psychiatry is a dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis in major depression (Holsboer, 2000). Many studies observed an increased production of the corticotropin-releasing hormone (CRH) in the hypothalamus, leading to an increased release of adrenocorticotropic hormone (ACTH) from the pituitary and subsequently to an enhanced production of cortisol in the adrenal cortex. Due to an impaired sensitivity of the glucocorticoid receptor (GR) the negative feedback mechanisms usually restoring homeostasis after a stress triggered cortisol release are not functioning properly (Holsboer, 2000, Pariante and Miller, 2001). However, treatment strategies targeting the GR or the CRH receptors have not been successful for a general patient population. Selecting the right patients for these treatment alternatives may improve therapy outcome, since a dysregulation of the HPA axis affects only 40-60 % of the depressed patients. Thus, patients with a dysregulated HPA axis have first to be identified and then allocated to a specific treatment regime. Tests like the dexamethasone-suppression-test (DST) or the dex-CRH test have been shown to uncover GR sensitivity deficits, but are not routinely applied in the clinical setting. Recently, the dexamethasone-induced gene expression could uncover GR alterations in participants suffering from major depression and job-related exhaustion (Menke et al., 2012, Menke et al., 2013, Menke et al., 2014, Menke et al., 2016). Actually, by applying the dexamethasone-stimulation test we found a GR hyposensitivity in depressed patients (Menke et al., 2012) and a GR hypersensitivity in subjects with job-related exhaustion (Menke et al., 2014). These alterations normalized after clinical recovery (Menke et al., 2014). Interestingly, the dexamethasone-stimulation test also uncovered FKBP5 genotype dependent alterations in FKBP5 mRNA expression in depressed patients and healthy controls (Menke et al., 2013). FKBP5 is a co-chaperone which modulates the sensitivity of the GR (Binder, 2009). In addition, the dexamethasone-stimulation test provided evidence of common genetic variants that modulate the immediate transcriptional response to GR activation in peripheral human blood cells and increase the risk for depression and co-heritable psychiatric disorders (Arloth et al., 2015). In conclusion, the molecular dexamethasone-stimulation test may thus help to characterize subgroups of subjects suffering from stress-related conditions and in the long-run may be helpful to guide treatment regime as well as prevention strategies.   References: Arloth J, Bogdan R, Weber P, Frishman G, Menke A, Wagner KV, Balsevich G, Schmidt MV, Karbalai N, Czamara D, Altmann A, Trumbach D, Wurst W, Mehta D, Uhr M, Klengel T, Erhardt A, Carey CE, Conley ED, Major Depressive Disorder Working Group of the Psychiatric Genomics C, Ruepp A, Muller-Myhsok B, Hariri AR, Binder EB, Major Depressive Disorder Working Group of the Psychiatric Genomics Consortium PGC (2015) Genetic Differences in the Immediate Transcriptome Response to Stress Predict Risk-Related Brain Function and Psychiatric Disorders. Neuron 86:1189-1202. Binder EB (2009) The role of FKBP5, a co-chaperone of the glucocorticoid receptor in the pathogenesis and therapy of affective and anxiety disorders. Psychoneuroendocrinology 34 Suppl 1:S186-195. Holsboer F (2000) The corticosteroid receptor hypothesis of depression. Neuropsychopharmacology 23:477-501. Menke A, Arloth J, Best J, Namendorf C, Gerlach T, Czamara D, Lucae S, Dunlop BW, Crowe TM, Garlow SJ, Nemeroff CB, Ritchie JC, Craighead WE, Mayberg HS, Rex-Haffner M, Binder EB, Uhr M (2016) Time-dependent effects of dexamethasone plasma concentrations on glucocorticoid receptor challenge tests. Psychoneuroendocrinology 69:161-171. Menke A, Arloth J, Gerber M, Rex-Haffner M, Uhr M, Holsboer F, Binder EB, Holsboer-Trachsler E, Beck J (2014) Dexamethasone stimulated gene expression in peripheral blood indicates glucocorticoid-receptor hypersensitivity in job-related exhaustion. Psychoneuroendocrinology 44:35-46. Menke A, Arloth J, Putz B, Weber P, Klengel T, Mehta D, Gonik M, Rex-Haffner M, Rubel J, Uhr M, Lucae S, Deussing JM, Muller-Myhsok B, Holsboer F, Binder EB (2012) Dexamethasone Stimulated Gene Expression in Peripheral Blood is a Sensitive Marker for Glucocorticoid Receptor Resistance in Depressed Patients. Neuropsychopharmacology 37:1455-1464. Menke A, Klengel T, Rubel J, Bruckl T, Pfister H, Lucae S, Uhr M, Holsboer F, Binder EB (2013) Genetic variation in FKBP5 associated with the extent of stress hormone dysregulation in major depression. Genes Brain Behav  12:289-296. Otte C, Gold SM, Penninx BW, Pariante CM, Etkin A, Fava M, Mohr DC, Schatzberg AF (2016) Major depressive disorder. Nature reviews Disease primers 2:16065. Pariante CM, Miller AH (2001) Glucocorticoid receptors in major depression: relevance to pathophysiology and treatment. Biological psychiatry 49:391-404.

NEUROINFLAMMATORY GENE EXPRESSION IN HIPPOCAMPUS IN MAJOR DEPRESSIVE DISORDER

2019 ◽  
Vol 29 ◽  
pp. S842
Author(s):  
Gouri Mahajan ◽  
Eric Vallender ◽  
Michael Garrett ◽  
Lavanya Challagundla ◽  
James Overholser ◽  
...  
Keyword(s):  
Gene Expression ◽  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Major Depressive

scholarly journals Altered choroid plexus gene expression in major depressive disorder

2014 ◽  
Vol 8 ◽  
Author(s):  
Cortney A. Turner ◽  
Robert C. Thompson ◽  
William E. Bunney ◽  
Alan F. Schatzberg ◽  
Jack D. Barchas ◽  
...  
Keyword(s):  
Gene Expression ◽  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Choroid Plexus ◽  
Major Depressive

scholarly journals Interleukin-6 Gene Expression Changes after a 4-Week Intake of a Multispecies Probiotic in Major Depressive Disorder—Preliminary Results of the PROVIT Study

Nutrients ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2575
Author(s):  
Alexandra Reiter ◽  
Susanne A. Bengesser ◽  
Anne-Christin Hauschild ◽  
Anna-Maria Birkl-Töglhofer ◽  
Frederike T. Fellendorf ◽  
...  
Keyword(s):  
Gene Expression ◽  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Interleukin 6 ◽  
Intervention Group ◽  
Additional Treatment ◽  
Major Depressive ◽  
Efficient Treatment ◽  
Expression Levels ◽  
Gene Expression Levels

Major depressive disorder (MDD) is a prevalent disease, in which one third of sufferers do not respond to antidepressants. Probiotics have the potential to be well-tolerated and cost-efficient treatment options. However, the molecular pathways of their effects are not fully elucidated yet. Based on previous literature, we assume that probiotics can positively influence inflammatory mechanisms. We aimed at analyzing the effects of probiotics on gene expression of inflammation genes as part of the randomized, placebo-controlled, multispecies probiotics PROVIT study in Graz, Austria. Fasting blood of 61 inpatients with MDD was collected before and after four weeks of probiotic intake or placebo. We analyzed the effects on gene expression of tumor necrosis factor (TNF), nuclear factor kappa B subunit 1 (NFKB1) and interleukin-6 (IL-6). In IL-6 we found no significant main effects for group (F(1,44) = 1.33, p = ns) nor time (F(1,44) = 0.00, p = ns), but interaction was significant (F(1,44) = 5.67, p < 0.05). The intervention group showed decreasing IL-6 gene expression levels while the placebo group showed increasing gene expression levels of IL-6. Probiotics could be a useful additional treatment in MDD, due to their anti-inflammatory effects. Results of the current study are promising, but further studies are required to investigate the beneficial effects of probiotic interventions in depressed individuals.

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